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Medicine block > Diabetes and endocrinology > Flashcards

Diabetes and endocrinology Flashcards

1
Q

Describe the thyroid gland anatomically and explain the way it moves

A

A L lobe and a R love joined together by an isthmus. Sits anterior to the thyroid cartilage within the neck. Moves on swallowing as thyroid cartilage moves on swallowing.

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2
Q

What remnant tissues can be left from the embryological migration of the thyroid?

A
  • Thyroglossal cyst

- Lingual thyroid

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3
Q

What structures can be damaged in thyroid surgery?

A

Recurrent laryngeal nerve - lies laterally on either side of the thyroid
Parathyroid gland - lies anteriorly

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4
Q

What is the blood supply of the thyroid?

A

Sup and inf thyroid arteries

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5
Q

How does the thyroid synthesise hormones and where does it store them?

A

Follicular cells secrete thyroglobulin - > thyroxine (T4) which is stored in colloid tissue.
C cells secrete calcitonin.

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6
Q

What is the difference between T3 and T4?

A

T4 in main circulation and is converted peripherally to short acting T3.

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7
Q

What are the actions of T3 and T4?

A
  • Increase BMR
  • Growth in childhood
  • Increase HR and increase peripheral vasodilation near the body’s surface
  • Increase myelination of nerves
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8
Q

What is the TFT of primary hypothyroidism?

A

Increased TSH and decreased T4.

Problem w the thyroid gland, often autoimmune.

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9
Q

What is the TFT of secondary hypothyroidism?

A

Decreased T4 and non elevated TSH.

Normally TSH def caused by pituitary disease.

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10
Q

What is the TFT of hyperthyroidism?

A

Increased T4 and T3, reduced TSH.

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11
Q

What factors affect TFTs?

A
  • Pregnancy
  • Lithium
  • Amiodarone
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12
Q

What are the causes of hyperthyroidism?

A
  • Grave’s
  • Nodular thyroid disease
  • Thyroiditis
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13
Q

What is Grave’s?

A

Autoimmune TSH receptors stim Ab. Relapsing and remitting disease, most common in young women.

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14
Q

What is nodular thyroid disease?

A

Excess secretion of T3+T4 from nodules within a toxic multi nodular goitre. More common in elderly people.

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15
Q

What is thyroiditis?

A

Inflam of the thyroid causes release of thyroxine. Caused by viral infection, childbirth and meds eg. amiodarone.

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16
Q

What are the clinical features of hyperthyroidism?

A 
Caused by increased sympathetic activity:
- Weight loss w increased appetitie
- Insomnia, irritability, anxiety
- Heat intolerance due to increased BMR
- Palpitations and tremor
Extra sx:
- Pruritis
- Diarrhoea
- Reduced fertility and menstrual irregularity
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17
Q

What are the presentations of hyperthyroidism in children and the elderly?

A

Children - accelerated growth and behavioural defects

Elderly pt - reduced energy levels

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18
Q

What are the signs of hyperthyroidism?

A
  • Tachycardia
  • Warm peripheries
  • Tremor
  • Hyper reflexia and lid lag
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19
Q

What causes lid lag?

A

Increase sympathetic activity in the upper eyelid. Superior tarsal muscle is supplied by sympathetics and aids levator palpebris superioris (oculomotor nerve) to elevate eye.

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20
Q

What are the specific signs of Grave’s disease?

A
  • Thyroid eye disease = lid retraction and proptosis
  • Pretibial myxoedema = red and swollen shins
  • Thyroid acropachy = clubbing
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21
Q

What are the hyperthyroidism TFTs?

A
  • Elevated T3 and T4 w nondetectable TSH

- Subclinical hyperthyroidism = normal T3/T4 and reduced TSH

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22
Q

What are the other Ix into hyperthyroidism?

A
  • Thyroid USS - can confirm if nodular thyroid disease but doesn’t measure thyroid activity
  • Nuclear imaging - detects cause of hyperthyroidism
  • Thyroid peroxidase Ab (TPO) is non specific marker for autoimmune disease, TSH receptor stim Ab is more specific
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23
Q

What are the medical treatments of hyperthyroidism?

A

Thionamides eg. carbamizole reduce the synthesis of T3/T4. They normally take 4-6 weeks to normalise TFTs and in the mean time a B blocker can be used to control sx.
If sore throat - need FBC, may have bone marrow suppression.

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24
Q

What are the SE of thionamides?

A
  • Generalised rash

- Bone marrow suppression - if unexplained fever or sore throat do FBC to see if pancytopenia - stop meds if neutropenia

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25
Q

What are the definitive treatments of hyperthyroidism?

A
  • Radioactive iodine

- Thyroidectomy

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26
Q

Describe using radioactive iodine as a treatment of hyperthyroidism

A

One single dose of 131 iodine.
Don’t use in pregnant women and don’t get close to pregnant women or children a few days after as pt becomes radioactive.
Can worsen thyroid eye disease and often causes hypothyroidism so pt will need life long thyroxine supplement.

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27
Q

What are the complications of a thyroidectomy?

A
  • RLN palsy as anatomically close
  • Hypocalcaemia due to hypoparathyroidism
  • Bleed, infection
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28
Q

What are the primary causes of hypothyroidism?

A
  • Autoimmune disease eg. Hashimoto’s
  • Drugs eg. amiodarone + lithium
  • Genetic defect reducing T3/T4 synthesis
  • Iodine def can cause in neonates and causes ‘cretinism’
  • Transient or perm after pregnancy + can be mis diagnosed as post natal depression
  • Iatrogenic - treatment for hyperthyroidism or radiation to neck
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29
Q

What are the secondary causes of hypothyroidism?

A

Less common than primary causes. TSH def due to hypothalamic pit disease = reduced T4 and non elevated TSH.

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30
Q

What are the clinical features of hypothyroidism?

A 
Sx similar to depression/chronic fatigue:
- Weight gain
- Cold intolerance
- Fatigue
- Bradycardia 
- Constipation
- Myxoedema around eyes
Most commonly an incidental finding.
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31
Q

What is Hashimoto’s thyroiditis?

A

Enlarged thyroid gland with hypothyroidism

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32
Q

What are the Ix into hypothyroidism?

A
  • TFT = reduced T4 and increased TSH (increased TSH enough to diagnose primary but need T4 to diagnose secondary)
  • Thyroid Ab to confirm autoimmune disease, TPO strongly positive in Hashimoto’s
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33
Q

What is the treatment of hypothyroidism? What are the problems of replacement?

A
  • Thyroxine replacement - 50-100 ug/day
  • Increased TSH = under replacement, non compliance of malabsorption
  • Reduced TSH = over replacement, increases risk of Afib and osteoporosis
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34
Q

What is subclinical hypothyroidism?

A
  • Normal T4 and increased TSH

- In this case asymptomatic pt doesn’t need treatment and thyroid func often spontaneously resolves

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35
Q

When should treatment be offered in subclinical hypothyroidism?

A
  • Symptomatic
  • Pregnant or planning
  • Dyslipidaemia
  • If +ve thyroid Ab annual TFTs to ensure don’t develop overt hypothyroidism
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36
Q

What are the parts of the adrenal gland?

A

Adrenal gland sits on top of the kidney and is made up of the adrenal medulla (centrally) and the adrenal cortex (on the outside).

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37
Q

What does the adrenal cortex secrete?

A

GAM:

  • Glucocorticoids
  • Adrenal androgens
  • Mineralcorticoids
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38
Q

What do glucocorticoids do? What hormone controls their release?

A

Cortisol is the main one and it has a role in metabolism, controlled by ACTH. -ve feedback on the hypothalamus to reduce CRH, ACTH and ADH.
Highest in the morning and lowest at night.
Is only biologically active when free but most in blood is bound.

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39
Q

What do adrenal androgens do?

A

Have a role in puberty and adult females, (male androgens from testes).
Act on the sebaceous glands, hair follicles, ex genitalia and prostate.

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40
Q

What do mineralcorticoids do?

A

Aldosterone is the main one, controlled by RAAS and stim by Ang2.
Acts on the DCT to increase Na retention and reduce K+ excretion.

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41
Q

What is the adrenal medulla?

A

Is made up of sympathetic NS and secretes adrenaline, noradrenaline and dopamine.

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42
Q

What is Addison’s and what causes it?

A

Primary adrenal insufficiency.

Causes - destruction of the adrenal gland or genetic defect in steroid synthesis. All 3 adrenal cortex affected.

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43
Q

What are the clinical features of Addison’s and why do pt get them?

A
  • Fatigue, weakness, anorexia, weight loss, nausea, abdo pain
  • Postural hypertension (reduced mineralcorticoids)
  • Hypoglycaemia (reduced glucocorticoids)
  • Increased pigmentation (increased ACTH as no neg feedback)
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44
Q

What are the Ix into Addison’s?

A
  • Low 9am cortisol

- Primary adrenal failure normally shows = low Na, high K, increased urea, hypoglycaemia and anaemia

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45
Q

What is the management of Addison’s?

A

Life long replacement of gluticorticoids = hydrocortisone or low dose prednisolone and mineralcorticoids = fludrocortisone.
Pt need to double G dose during illness and need to take IV in surgery, diarrhoea or vom.

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46
Q

What is an Addisonian crisis? How is it treated?

A 
Features = collapse, coma, dehydration, hypotension, increased pigmentation. 
Treat = IV fluids and hydrocortisone.
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47
Q

What is the cause of secondary adrenal insufficiency?

A

ACTH deficiency - can be caused by long term steroid use which suppresses ACTH. Sudden stopping of steroids can cause an adrenal crisis.

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48
Q

What are the disorders of the adrenal medulla?

A
  • Phaeochromocytoma

- Paraganglioma

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49
Q

What are phaeochromocytomas and paragangliomas?

A

Tumours that release excess catecholamines.

Phaeochromocytoma stems from the adrenal medulla but a paraganglioma stems from extra adrenal chromaffin tissue.

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50
Q

When are disorders of the adrenal medulla suspected to have a familial link?

A
  • When a pt presents at a young age
  • When the tumour is bilateral, malignant or extra adrenal
    Will need to do genetic testing to confirm.
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51
Q

What are the clinical features of paheochromocytomas and paragangliomas?

A
  • Sweating
  • Palpitations, anxiety, panic attacks
  • Headaches
  • 90% have HTN
  • If untreated = hypertensive crisis
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52
Q

What are the clinical features of a hypertensive crisis?

A

Huge HTN with organ damage - encephalopathy, pulm oedema, hyperglycaemia, cardiac arrhythmia. Can cause death.

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53
Q

What are the Ix into phaeochromocytomas and paragangliomas?

A
  • 24 hr catecholamine and plasma metanephrine (will be elevated)
  • CT/MRI to localise tumour, abdo normally but can do full body
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54
Q

What is the definitive management of phaechromocytomas and paragangliomas?

A

Surgical excision, either lapro or open = removal of one or both of the adrenal glands.

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55
Q

What is the medical management of phaechromocytomas and paragangliomas? What order do you do it in?

A

All pt diagnosed with either need to be on a/B blockade.
a = phenoxybenzamine or doxazosin. Do a first to avoid a adrenergic stim which could cause HTN crisis. Add B blocker to control tachycardia if needed.

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56
Q

Draw the anatomy of the pituitary gland and label nearby structures

A

Answers on iPad

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57
Q

What is within the cavernous sinus?

A 
Cranial nerves:
- 3 = oculomotor
- 4 = trochlear
- 6 = abducens 
- Va and b branches of trigeminal (5)
and the int carotid artery.
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58
Q

What are the 5 pituitary axes?

A
  1. Growth axis
  2. Thyroid axis
  3. Gonadal axis
  4. Prolactin axis
  5. Adrenal axis
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59
Q

Describe the growth axis and the hormones job

A

Growth hormone - growth in children and maintaining healthy muscle in adults. At the liver produces IGF-1 which is a marker for GH.
+ve control = GHRH
-ve control = somatostatin

60
Q

Describe the thyroid axis and the hormones jobs

A

TSH released and acts on thyroid to release thyroxine.
+ve control = TRH
-ve control = thyroxine

61
Q

Describe the gonadal axis and the hormones jobs

A

LH = ovulation and corpus luteum in women, testosterone from Leydig cells in men.
FSH = ovarian follicle in women, sperm synthesis in men.
+ve control = GnRH
-ve control = testosterone and oestrogen
Prolactin directly inhibits LH and FSH.

62
Q

Describe the prolactin axis and the hormones jobs

A

Prolactin causes lactation and directly inhibits LH and FSH.
+ve control - TRH a bit
-ve control - dopamine, anything that blocks dopamine increases prolactin

63
Q

Describe the adrenal axis and the hormones jobs

A

ACTH high in the morning and low at night, causes cortisol release.
+ve control - CRH
-ve control - cortisol

64
Q

What are the clinical sign of pathology of the pituitary gland?

A

Pit tumours present due to compression of adjacent structures or excess of hormones:

  • Compression of optic chiasm = bi temporal hemianopia
  • Hormone excess = Cushing’s, acromegaly, hyperprolactinoma, hypopituitism
65
Q

What is the indication for surgery on the pit gland?

A

Optic chiasm compression causing bi temporal hemianopia

66
Q

What are the basal biochem tests for assessing the pit gland?

A
  • IGF-1 is the marker for GH
  • FSH + LH should be measured in a womens first 5 days of menstrual cycle and at 9am for men
  • Cortisol at 9am
  • Prolactin and TSH can check at any time of day
67
Q

What are the dynamic bio chem tests?

A
  • Insulin tolerance test

- Synacthen test (synthetic ACTH)

68
Q

What is the synacthen test?

A

When there has been ACTH def for 2 weeks+ there is atrophy of the adrenal cortex and it will no longer be stim to make cortisol by the synacthen.

69
Q

What is the insulin tolerance test?

A

If you get hyperglycaemia with symptoms GH and ACTH will increase - not sure I understand this.

70
Q

What imaging is used in the assessment of the pit gland?

A

MRI w contrast - should be able to differentiate between the tumour and the gland.
>1 cm = macro
<1 cm = micro

71
Q

What are the alternative causes of hyperprolactinaemia (not prolactinoma)?

A
  • Pregnancy
  • PCOS
  • Profound hypothyroidism but is rare
  • Dopamine antagonists eg. anti emetics and anti psychotics
72
Q

What are the demographics and presentation of a microprolactinoma? How does a macroprolactinoma differ?

A

Micro = women > men
Macro = men > women
Presentation - menstrual disruption, infertility, galactorrhoea, hypogonadism in men

73
Q

How can you differentiate between PCOS and microprolactinoma?

A

In PCOS there is androgenic sx, PRL is normally <1000 iU/L and there is no pit lesion found on MRI.

74
Q

What level of prolactin suggests an active prolactin secretion?

A

> 5000 iU/L

75
Q

What is the treatment of hyperprolactinaemia?

A

Dopamine agonists - cabergoline (1/2 times a week so better tolerated) or bromocriptine (every day).

76
Q

What are the side effects of dopamine agonists to treat hyperprolactinaemia?

A
  • Nausea
  • Postural hypertension
  • Psych disturb
77
Q

What are the causes of acromegaly?

A

GH secreting pit tumour

78
Q

What is the appearance of a person with acromegaly?

A
  • Increased size of hands and feet
  • Prominent forehead and chin, gapped teeth
  • Soft tissue inflam = large tongue and soft palate = sleep apnoea and swollen hands = carpal tunnel syndrome likely
79
Q

What are the clinical features of acromegaly unrelated to appearance?

A
  • Sweating
  • Headaches
  • HTN
  • Diabetes mellitus
80
Q

What are the risks of leaving acromegaly untreated?

A
  • Facial deformities/disfiguring features

- CVS disease and death

81
Q

What are the ix into acromegaly?

A
  • Oral glucose tolerance test
  • Measure IGF-1 levels, elevated
  • Pit MRI - will usually see pit tumour
82
Q

What is a co secreting tumour in acromegaly?

A

Often the GH secreting pit tumour will also secrete prolactin, so will also have raised PRL

83
Q

What is an OGTT?

A

Oral glucose tolerance test = measure GH before and then give pt a sugary drink, if GH isn’t decreased pt has acromegaly.
Glucose should normally cause a decrease in GH.

84
Q

What is the management of acromegaly?

A
  • Surgical = remission more likely in microadenomas than macroadenomas
    Medical:
  • Stereotactic RT
  • Somatostatin analogues by monthly injection
  • GH receptor blockers
85
Q

How do you monitor acromegaly?

A
  • After surgery = measure GH to see if persistent disease
  • Colonoscopy screening as acromegaly increases risk bowel cancer
  • Screen for sleep apnoea, DM and CVS risk
86
Q

What is a non functioning pit adenoma?

A

A biochemically inactive tumour but instead causes sx by compression = hypopituitarism, visual field loss and headache.

87
Q

When is surgery on a NFPA indicated?

A

Causing visual field loss or a threat to vision

88
Q

What are the causes of hypopituitarism?

A
  • Acquired = pit tumour, inflam or infiltrative disease, traumatic brain injury, RT
  • Congenital, present when young
89
Q

What are the sx of hypopituitarism?

A
  • Lethargy
  • Weight gain
  • Sexual dysfunction
  • Short stature in children
90
Q

What should you suspect in a pt w pit disease and a reduced QOL? What is the pt composition like?

A

Suspect GH def - reduced muscle and bone mass with increased fat

91
Q

What are the ix into hypopituitarism?

A
  • Reduced T4, non elevated TSH
  • Reduced sex hormones, non elevated LH and FSH
  • IGF-1 reduced
  • Tumour on MRI
92
Q

What is the treatment of hypopituitarism?

A
  • ACTH def = hydrocortisone
  • TSH def = throxine
  • GH def = daily GH injections
  • Sex hormone def = testosterone infections in men and O+P in women, COCP or HRT
93
Q

What is needed to confirm a DKA diagnosis?

A
  • BM >11 mmol/L or known DM
  • Ketonuria >2 or blood ketones >3 mmol/L
  • pH <7.3 or bicarb < 15 mmol/L
94
Q

What is the immediate management of DKA?

A
  • AtoE - RR, pulse oximetry, pulse, BP, temp, EWS, GCS
  • Set up IV access
  • Cap blood glucose and blood ketones
  • Urinalysis for ketones
  • Bloods - FBC, U&Es, blood ketones, bicarb
95
Q

What actions do you take after the immediate management of DKA?

A
  • IV fluid prescription - 0.9% NaCl
  • 10 units insulin STAT, then continual fixed rate infusion
  • K+ replacement = 20 mmol in 500 ml
  • Glucose infusion to prevent hypoglycaemia, 5% dextrose
96
Q

Give some detail for IV fluid prescribing in DKA

A 
If systolic BP over 90mmHg:
1st = 1L NaCl 0.9% over 1 hour then..
- 1L over 2 hrs x2
- 1L over 4 hrs x2
- 1L over 6 hrs x2
If systolic BP under 90mmHg - NaCl 0.9% 500ml over 15 mins.
97
Q

How do you monitor a pt w DKA?

A
  • After 1 hour do cap blood glucose and U&Es

- Cont pulse oximetry and cardiac monitoring if required

98
Q

What are the indications of severe DKA?

A
  • GCS <12
  • Pulse >100 or <60 BPM
  • BP <90mmHg systolic
  • O2 sats <92%
  • pH <7
  • Hypokalaemia on admission
99
Q

What are the signs and symptoms of DKA?

A

Sx - palpitations, sweat, thirst, weight loss, N+V, abdo pain
Signs - tachy, hypotension, reduced skin turgor, Kassmaull breathing, dry mucous membrane, reduced urine output and consciousness

100
Q

What are the causes and RF of DKA?

A
  • BM constistently >15 mmol/L
  • Missing insulin injections or a fault w insulin pen
  • Infection
  • Excess alcohol consumption or illegal drug use
  • Prolonged period of stress
101
Q

What is HHS?

A

Hyperosmolar hyperglycaemic state. Occurs in T2DM and is a combination of dehyrdration and illness.
Skipping meds in illness or hormones in illness cause hyperglycaemia.

102
Q

What is the triad of HHS?

A
  1. Hyperglycaemia >30mmol/L
  2. Absence of significant acidosis
  3. High serum osmolality >320 mosmol/Kg
103
Q

What are the sx of HHS?

A
  • Thirst and dry mouth+skin
  • Nausea
  • Urination
  • Alt consciousness
104
Q

What is the management of HHS?

A
  • Insulin at a fixed rate infusion
  • Monitor K+ and replace when necessary
  • IV fluid prescription according to protocol and w caution in elderly to avoid fluid overload
  • LMWH for prophylaxis
  • Find and treat underlying cause
105
Q

What is the diagnostic criteria for T1DM?

A
  • Symptoms + one abnormal result or two abnormal results on two different times
  • Sx = weight loss, polydipsia, polyuria, fatigue
  • > 7 mmol/L fasting glucose or >6.5% HbA1c
106
Q

Give an overview of the pathophysiology of T1DM

A

Autoimmune destruction of B cells in pancreas (produce insulin), associated w other autoimmune diseases eg. thyroid disease and Addison’s.

107
Q

What is LADA syndrome?

A

Latent autoimmune diabetes in adults = insidious presentation of T1Dm

108
Q

Give an overview of the pathophysiology of T2DM

A

Insulin resistance due to hyperglycaemia = B cells increase insulin production but eventually give up and there is decreased B cell function.

109
Q

What are some of the other types of diabetes?

A
  • Pancreatic related = T3DM eg. chronic pancreatitis
  • Drugs
  • Endocrine causes - Cushing’s, acromegaly
  • MODI - monogenic cause
  • Gestational causes
110
Q

What are the drugs used in the treatment of T2DM?

A
  • Metformin, reduces hepatic glucose production, don’t use if CKD <30ml/min
  • SU, increase B cell insulin release, cause weight gain and hypoglycaemia
  • GLP agonists, increases insulin and satiety = weight loss and DPP-4 inhibitors stop breakdown of incretin which increases insulin, weight neutral
  • Anti obesity drugs = orlastat
  • SGLT-2 inhibitors, inhibits reabsorption of glucose at PCT
111
Q

What are the complications of diabetes?

A
  • Acute = hypoglycaemia, DKA, HHS
  • Chronic = microvascular = nephropathy, neuropathy, retinopathy, macrovascular = cerebrovascular, peripheral vascular, cardiovascular eg. Charcot’s foot
112
Q

What are the complications of DKA and HHS?

A 
DKA:
- Cerebral oedema
- Electrolyte disturbances = hypokalaemia
HHS:
- Arterial thrombosis
- Cerebral oedema
113
Q

How do you calculate osmolality?

A

2Na + glucose + urea

114
Q

What are the symptoms of hypoglycaemia?

A

<4mmol/L

  • Sweating, palpitations, shaking, hunger
  • Confusion, drowsiness, odd behaviour, speech difficulty, incoord
  • Headache, nausea
115
Q

What are the clinical features of Cushing’s syndrome?

A
  • Central obesity, dorso cervical fat pad, rounded face
  • Plethera (red face)
  • HTN, DM, osteoporosis
  • Thin skin and easy bruising
  • Proximal myopathy
116
Q

What are the Ix into Cushing’s?

A
  • Low dose dexamethasone suppression test and overnight dexamethasone suppression test = if don’t suppress cortisol = Cushing’s
  • 24 hr urine cortisol = elevated is Cushing’s
  • Need to rule out alcoholism and depression = pseudo Cushing’s
117
Q

What is the difference between Cushing’s syndrome and disease?

A

Cushing’s syndrome = any cause of excess cortisol, from outside or inside the body
Cushing’s disease = specific type of Cushing’s syndrome caused by ACTH producing pit adenoma

118
Q

What are the different causes of Cushing’s syndrome?

A
  • Pit adenoma = ACTH normal or high, +ve for tumour on pit MRI
  • Adrenal ACTH secreting tumour = ACTH low, hirsuitism
  • Ectopic ACTH, a paraneoplastic syndrome from cancer, normally lung
119
Q

What signs are suggestive of ectopic ACTH?

A
  • Hypokalaemia
  • History of smoking
  • Weight loss
120
Q

What is the management of each cause of Cushing’s syndrome?

A
  • Pit = trans sphenoidal removal of the pit gland
  • Adrenal = lapro adrenelectomy
  • Ectopic ACTH = treat underlying malignancy + medical management of cortisol if needed
121
Q

What drugs are used for the medical control of cortisol levels?

A
  • Metyrapone = inhibits cortisol

- Ketoconazole = prevents ACTH secretion

122
Q

What are the early signs of hyponatraemia?

A

Drowsiness, confusion and agitation

123
Q

What are the consequences of acute severe hyponatraemia and how is it managed?

A

Seizures, resp depression, coma, death.

Have to give hypertonic saline solution to avoid cerebral oedema but it is a senior decision.

124
Q

What are the ix into hyponatraemia?

A
  • Urine and serum osmolality
  • Urine Na
  • TFTs
  • 9am cortisol (ACTH def + Addison’s can cause)
  • Drug hx important as thiazide like diuretics can cause
125
Q

What are some of the causes of hyponatraemia? Characterise by fluid status

A

Hypovolaemic - burns, sweat, V+D, Addison’s
Euvolaemic - SIADH, hypothyroidism
Hypervolaemic - renal, heart, liver fail, nephrotic syndrome

126
Q

What is SIADH and what are the causes?

A

Syndrome of inappropriate ADH = too much water reabsorbed.
Causes = lung malignancy and can be other malignancies, anticonvulsants
Need to exclude ACTH def as it looks exactly the same by causing excess vasopressin secretion.

127
Q

What is the management of hyponatraemia?

A
  • Hypovolaemic hyponatraemia = normal saline
  • Hypervolaemic hyponatraemia = treat underlying cause
  • SIADH = reverse the cause, fluid restriction, ADH antagonists
128
Q

What is diabetes insipidus?

A

Producing large volumes of dilute urine w an excessive thirst. Increased serum osmolality and reduced urine osmolality
If severe = hypernatraemia, dehydration and death.

129
Q

Cranial DI vs nephrogenic DI

A

Cranial - ADH def, pit disease

Nephrogenic DI - ADH resistance, caused by metabolic or electrolyte disturbances, can be caused by lithium

130
Q

What can masquerade as DI?

A

Primary polydipsia = excessive thirst and drinking causes polyuria

131
Q

What are the Ix into DI?

A
  • Urine vol >3L over 24 hrs = DI
  • Water deprivation test = unacceptable thirst and lose weight due to water loss indicates DI, then give synthetic ADH and urine vol decreased (cranial DI, no effect in nephrogenic)
132
Q

How do you manage cranial DI?

A

Give synthetic vasopressin = desmopressin, can be administered orally, nasally, parentrally and sublingually.

133
Q

How can you tell if you have under treated or over treated DI?

A

Over treated = dilutional hyponatraemia, headache and reduced cognition
Under treated = excess thirst and polyuria

134
Q

How do you manage nephrogenic DI?

A
  • Treat any underlying cause
  • If still SE = pt should drink according to thirst to recover water loss
  • Low salt, low protein diet can help
135
Q

What are the causes of hypercalcaemia w decreased PTH?

A
  • Malignancy, SCC secretes PTHrP and causes hypercalcaemia

- Can also be caused by granulomatas eg. TB and sarcoidosis

136
Q

What are the causes of hypercalcaemia w normal PTH?

A

Primary hyperparathyroidism until proven otherwise, usually caused by a single pit adenoma. If there is pit hyperplasia in >1 gland then normally genetic eg. MEN

137
Q

What are the clinical features of hypercalcaemia?

A
  • Normally found incidentally as often asymptomatic
  • Vague sx = tiredness, generalised aches and pains
  • Specific sx = constipation, abdo pains, kidney stones, polyuria and polydispisa due to nephrogenic DI (hypercalcaemia can cause but don’t know why)
138
Q

What is FHH?

A

Familial hypocalciuric hypercalcaemia = reduced Ca:creatinine ratio w normally a FH of hypercalcaemia due to defect in Ca sensory receptor

139
Q

How can you treat hyperparathyroidism medically?

A

Calcimimetic drugs eg. cinacalcet that lowers Ca

140
Q

What are the causes of hypocalcaemia?

A
  • Post surgical hypo PTH after thyroidectomy
  • Vit D def, reduced Ca and phosphate, increased PTH
  • Hypomagnesaemia, func hypoPTH w normal/low PTH due to alcohol and drugs esp PPI
141
Q

What are the clinical features of hypocalcaemia?

A
  • Acute severe = laryngospasm, prolonged QT interval, seizures
  • Muscle cramps and carpo pedal spasm
  • Periorbital and peripheral paraesthesia
  • Neuropsych sx
142
Q

What is the treatment of hypocalcaemia?

A
  • Treat underlying cause
  • Acute = IV Ca
  • Vit D = cholecalciferol
  • HypoPTH = calcitrol and oral Ca2 supplements
  • Mg def = acute IV Mg or check why there is GI loss
143
Q

What are the triad of conditions in MEN-1?

A
  • Pancreatic tumours
  • Parathyroid hyperplasia
  • Pit tumours
144
Q

What is the treatment of hypoglycaemia?

A
  • A to E approach
  • IM glucagon or 75ml 20% glucose over 15 minutes
  • Stop insulin and don’t restart until BM >4mmol/ml
145
Q

What are the causes of hypoglycaemia in a diabetic?

A
  • Not eating enough carbs/increased exercise without carb adjustment
  • Illness/stress
  • Excessive alcohol consumption
  • Overuse of insulin
146
Q

What are the causes of hypoglycaemia in a non diabetic?

A
  • Alcoholism
  • Pancreatic insufficiency eg. CF or pancreatic tumour
  • Anorexia/skipping meals
  • Serious illness
  • Adrenal pit disorder
  • Hepatitis
147
Q

What is the treatment of unbalanced Na?

A

Hypernatraemia - dextrose or 0.45% saline, hypotonic

Hyponatraemia - normal saline 0.9%, hypertonic

Medicine block (8 decks)

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